Our primary aim is to develop novel moieties for the reinforcement of human blood platelet membranes and, thereby, reduce their susceptibility to impairments known to trigger adhesion-release-aggregation reactions. The thrust of these efforts will be directed particularly at difficulties experienced by persons bearing prosthetic devices which are in contact with their blood or by patients whose blood is exposed to biomaterials in the process of renal dialysis, blood oxygenation, cardiac catheterization, etc. In these individuals, the envisioned synthetic entities could significantly contribute to the maintenance of blood platelet membrane integrity during biodynamic impacts associated with increased probabilities of thrombus formation. The projected investigation would yield another important dividend. It should enable the investigators to identify molecular segments and functions capable of disrupting the texture of platelet membranes. Such information is not only essential for the development of effective and safe antithrombotic agents, but could become of critical importance in the selection of monomeric molecular constituents for biomaterials; eventually, it could facilitate a rational design of polymers void of functional groups with a potential to adversely affect platelets and, thereby, reduce or minimize the incidence of biomaterial-induced thromboembolic complications. Therefore, the molecular entities selected for the systematic study of chemical functions affecting platelet mebrane integrity constitute a pattern of gradual structural changes ranging from endogenous substances like alpha-tocopherol, known to exert membrane-stabilizing effects, to newly conceptualized synthetic compounds which should be capable of disrupting the platelet surface. The nature and extent of the effect exerted by the carefully selected entities will be assessed (1) on intact isolated human blood platelets and (2) on representative membrane constituents in monomolecular-film systems. Impacts on platelets will be studied through the compounds' capability to reduce or enhance (1) ADP-, thrombin-, and collagen-induced aggregation, (2) platelet retention by conventionally used biomaterials (e.g., polydimethylsiloxane, Cuprophane), and (3) release of platelet lactate dehydrogenase. In (a) interfacial-tension determinations, and (b) in monomolecular-film systems of arachidonic acid, of cholesterol and (Text Truncated -Exceeds Capacity)